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Arsenic-mediated activation of EGFR signaling pathway. EGFR and several components of this pathway can be activated by arsenic exposure in human lung cells. This activation can be inhibited by EGFR-TKI, revealing a potential role for TKIs in the management of arsenic associated lung tumors, regardless of the mutational status of EGFR. AsIII can also induce STAT3 inhibition by targeting JAK, while it can activate STAT3 trough JNK, contributing to AKT activation.
